Journal
NEURON
Volume 87, Issue 5, Pages 976-988Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2015.08.022
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Funding
- JPB Foundation
- Parkinson's Disease Foundation [NIH NIDA10154]
- Udall Center of Excellence for Parkinson's Disease research at Columbia University
- Swedish Research Council
- Sweden-America Foundation
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Degeneration of dopamine (DA) neurons in Parkinson's disease (PD) causes hypokinesia, but DA replacement therapy can elicit exaggerated voluntary and involuntary behaviors that have been attributed to enhanced DA receptor sensitivity in striatal projection neurons. Here we reveal that in hemiparkinsonian mice, striatal D1 receptor-expressing medium spiny neurons (MSNs) directly projecting to the substantia nigra reticulata (SNr) lose tonic presynaptic inhibition by GABAB receptors. The absence of presynaptic GABAB response potentiates evoked GABA release from MSN efferents to the SNr and drives motor sensitization. This alternative mechanism of sensitization suggests a synaptic target for PD pharmacotherapy.
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